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1、休 克,Shock,南昌大学一附院急诊科游,You,Emergency Department the First Affiliated Hospital of NanChang University,休克的历史沿革（History of shock）,Development of the concept of shock,A history of the 200 years to recognize shock:“shake”, “attack”From superficial syndrome to microcirculatory level , cellular level, molec
2、ular levelCirculatory level： blood pressureMicrocirculatory level： inadequate tissue perfusionCellular level and molecular level：FrontierExploratory stage，experimental therapies,机体在严重失血失液、感染、创伤等强烈致病因素作用下，有效循环血量急剧减少，组织血液灌流量严重不足，导致各重要生命器官和细胞的功能代谢障碍及结构损害的全身性病理过程。休克是一急性的综合征。在这种状态下，全身有效血流量减少，微循环出现障碍，导致重要
3、的生命器官缺血缺氧。即是身体器官需氧量与得氧量失调。,Concept,Shock is a dangerous systemic pathologic process under the effect of various drastic etiological factors, characterized by acute circulatory failure including decreased effective circulatory blood volume, inadequate tissue perfusion, cellular metabolism impediment
4、and dysfunction of multiple organs.,Simply.,oxygen requirement,oxygen delivery,1病因（Etiology）,ETIOLOGY AND CLASSIFICATION,【血液动力学分类】（Classification by hemodynamics）,2.分类（Classification by initial changes ）,Hypovolemic shock (Decreased blood volume)低血容量性休克各种病因引起的机体血容量减少所致的休克。Vasogenic shock (low-resist
5、ance shock or distributive shock)血液分布性休克外周血管扩张，血管床容量增加，大量血液淤滞在扩张的小血管内，使有效循环血量减少而引起的休克。Cardiogenic shock (Inadequate cardiac output)心源性休克由于心泵功能障碍，心输出量急剧减少，有效循环血量和微循环灌流量显著下降所引起的休克。Obstructive shock (obstruction of blood flow outside of the heart ) 阻塞性休克,Distributive (hyperdynamic) Shock,Hyperdynamic s
6、tate with high cardiac outputNormal to low filling pressuresDecreased systemic vascular resistanceMixed venous oxygen may be normal or increased,Distributive (hyperdynamic) Shock,causes:SIRS (sepsis, burns, trauma, pancreatitis)neurogenic (spinal trauma)anaphylaxis / anaphylactoidendocrine (thyroid,
7、 myxoedema, adrenal)pharmacologic (vasodilators, benzodiazepines),Hypovolaemic Shock,LV preload is too low to support adequate stroke volumecompensatory mechanisms: tachycardia, increased venous tone, increased vascular resistance, increased contractility, decreased urine output and Na+ reabsorption
8、 may help compensate for up to 1.5 L of blood lossshock develops when blood loss exceeds 20-25% of normal circulating volumeprolonged hypovolaemic shock leads to metabolic acidosis, then cardiogenic shock,Hypovolaemic Shock,causes:blood losspolyuriaGI lossburnsvasodilationthird space lossesvascular
9、permeability,Obstructive Shock,causes:tension pneumothoraxpulmonary emboli (thrombo-, air-, amniotic)mediastinal tumourspericardial tamponade, constrictive pericarditisacute pulmonary hypertensionaortic dissectionvalvular (mitral stenosis, aortic stenosis)vena-caval compression,Cardiogenic Shock,car
10、diac index below 2 L/min/m2PCWP greater than 17-20 mmHg,Cardiogenic Shock,causes:ischaemiamyocardial contusionvalvular diseasecardiomyopathymyocarditisdysrhythmiassepticaemiapharmacologic,various shock states may interrelate clinically to produce a mixed picturehypovolaemic shock may lead to acidosi
11、s and result in cardiogenic shockseptic shock may lead to hypovolaemia as a result of microbial toxins, cytokines, and capillary permeability,The Shock Cycle,The Shock Cycle,Consequences of Shock,hypothermiacoagulopathyacid-base disturbanceselectrolyte abnormalitiescellular injury and Multi-System O
12、rgan Failuredeath,PATHOGENESIS OF SHOCK,微 循 环 机 制MICROCIRCULATION MECHANISMS,细 胞 分 子 机 制CELLULAR AND MOLECULAR MECHANISMS,微循环的组成微动脉、后微动脉毛细血管前括约肌真毛细血管通血毛细血管（直捷通路）动-静脉吻合支微静脉。,直捷通路：微动脉 后微动脉和通血毛细血管 微静脉迂回通路：微动脉 后微动脉 毛细血管前括约肌 真毛细血管网 微静脉动静脉短路：微动脉 动静脉吻合支 微静脉,前、后阻力血管的特点两点同：1.对儿茶酚胺的敏感性不同2.对缺氧酸中毒的耐受性不同,1. Alte
13、rations of microcirculation perfusion（微循环变化的特点）少灌少流或少灌多流；微循环缺血、缺氧。 fluid and no perfusion,图2 微循环休克早期,（一）休克代偿期（Compensatory stage）,微循环变化的机制,减压反射窦弓反射,血管收缩,前阻力大于后阻力灌少流多,动静脉吻合支开放,大出血血容量减少心输出量下降血压下降,缺血缺氧,交感肾上腺（+）儿茶酚胺释放,血管紧张素管加血压素血栓素A2心肌抑制因子,Compensatory mechanisms (early shock),休克早期微循环的代偿,1）血容量增加 组织液回流加速
14、 2）心输出量增加 回心血量增加 心肌收缩增强 心率加速3）维持动脉血压 心输出量增加 外周阻力增加4）血流重新分布,Compensatory mechanisms,precapillary resistance vessel to contract，to decrease capilary hydrostatic pressure.,fluid and no perfusion,CNS ,烦燥不安神志清楚,休克病因,交感肾上腺髓质,休克早期的临床表现,交感-肾上腺髓质系统兴奋和儿茶酚胺大量释放是不同类型休克的共同通路。,血管收缩无选择性,（3）代偿意义（Compensatory signif
15、ication ） 动脉血压的维持（Maintain arterial blood pressure）,缺血缺氧期的临床表现 （Clinical manifestation in Ischemic hypoxia stage） 脸色苍白、 四肢冰凉、尿量减少（多为功能性急性肾衰） 脉搏细速、脉压减少 烦燥不安、出冷汗 血压可急降(失血)、也可微降，甚至正常(代偿),mild tachycardia; bounding pulseLevel of Consciousness: lethargy, confusion, combativenessSkin: delayed capillary re
16、fill; cool and clammyBlood Pressure: normal or slightly elevatedRespirations: rapid and shallow,Early Stage (compensated shock): Compensatory mechanisms are able to maintain perfusion of vital organs,The ischemic hyoxia stage is a reversible com- pansatory stage. Eliminating pathogenic factors and r
17、estoring blood volume and tissue perfusion are re- commended. Otherwise, it may progress to a more advanced stage.,1. Alterations of microcirculation perfusion（微循环变化的特点）多灌少流、灌大于流；微循环淤血、缺氧。,图3 微循环休克期,（二）休克失代偿期（Reversible decompensatory stage）,淤血缺氧,微循环淤血的机理,组织胺 激肽类腺苷 内毒素等,缺血缺氧 酸中毒,前阻力血管对儿茶酚胺反应性降低,前阻力血
18、管扩张,灌多,流少,后阻力血管收缩,后阻力血管对酸中毒耐受性强,血管扩张通透性,血液浓缩流速缓慢,微循环淤血,微血管扩张通透性,心输出量下降血压下降,缺氧酸中毒组织胺激肽 内毒素腺苷内啡肽等,回心血量急剧下降,滤出大于回流,更严重缺氧,毛细血管压增高,微循环淤血的后果,微循环淤血,血压,休克期临床表现,回心血量减少,脑缺血,血压,肾血流量减少,心输出量减少,皮肤淤血,肾淤血,皮肤紫绀出现花斑,神智淡漠、昏迷,少尿无尿,心博无力心音低钝脉搏细速静脉塌陷,Middle Stage (uncompensated shock):Compensatory mechanisms are unable to
19、 maintain perfusion,Heart Rate: moderate tachycardia; weak and thready pulseLevel of Consciousness: confusion or unconsciousnessSkin: delayed capillary refill; cold, clammy, and cyanoticBlood Pressure: decreasedRespirations: rapid and shallowUrine output: oliguria,2失代偿机制（Mechanisms of decompensation
20、）,（1）神经-体液机制,参与扩血管或增加血管通透性的主要产物组 胺 作用H2受体、引起血管扩张、cap通透性腺 苷、 K+ ATP产物，细胞释出K+ ，组织液渗透压激肽 激肽类物质、引起扩血管扩张内源性阿片类 调节心血管系统的神经肽有：TRF、 CRF （内啡肽） 抑制心功能、降低血压、减慢心率血小板活化因子 增强血小板聚集和释放；趋化白细胞、粘附于 （PAF） 微静脉；增强毛细血管通透性肿瘤坏死因子 激活白细胞；诱导PAF、CT4、TXA2、溶 （TNF) 酶体酶、自由基；诱导内皮细胞粘附受体； 诱导合成EDRF,（2）血液流变学的改变（Changes of blood rheology）
21、,血浆流态改变,心脑血液灌流减少（Decreased of perfusion to heart, brain）,图4 微循环休克晚期,1. Alterations of microcirculation perfusion（微循环变化的特点）不灌不流 微血管麻痹性扩张、微血栓形成、血流停止,（三）休克难治期（Refractory stage）,DIC发生机理及影响,血管内皮损伤血小板激活血液浓缩流速缓慢等,血液高凝状态,血液低凝状态,微血栓形成,回心血量急剧减少,心输出量急剧下降,血压急剧下降,大脑缺血,出血,3. 淤血性缺氧期的临床症状（Clinical manifestation in
22、stagnant hypoxia stage ） 血压进行性7 kPa、心搏无力、心音低钝 静脉淤血、血细胞压积、皮肤紫绀、花斑 少尿、无尿（器质性肾衰） 昏迷,Late Shock,Heart Rate: bradycardia; severe dysrhythmiasLevel of Consciousness: comaSkin: pale, cold, marked diaphoresisBlood Pressure: marked hypotensionRespirations: decreased rate and tidal volumeUrine output: oliguri
23、a or anuria,multiple system organ failure, MSOF,Irreversible shock,Hypercoagulable character erythrocyte and thrombocyte to aggregate,DIC,Cellular hypoxia，lysosome rupturehydrolytic enzyme releasing,aqtocytolysis and to damage other cells,Cell damage, organ failure occur,death occur,no perfusion and
24、 no fluid,3. 休克难治期的临床表现（Clinical manifestation in Microcirculatory failure stage）失代偿期症状加重等。,循环衰竭：进行性顽固性血压，脉细弱速，静脉塌陷， CVP。,DIC：身遍瘀斑,MOSF：呼吸困难；无尿；大脑缺血：神志不清,休克发展过程中微循环三期的变化,休克期 休克期 休克期,特点,机制,影响,decrease in BP 90 mmHg systolic or a fall of 30-40 mmHgdecreased cerebral blood flow with obtundation or rest
25、lessnessdecreased renal blood flow/pressure with oliguriadecreased peripheral blood flow with cool mottled periphery (except in sepsis),Diagnosis of Shock,休克的诊断,作为临床综合征，休克的诊断，常以低血压、微循环灌注不良、交感神经代偿性亢进等方面的临床表现为依据。诊断条件：有发生休克的病因；意识异常；脉搏快超过100次min，细或不能触及；四肢湿冷，胸骨部位皮肤指压阳性（压后再充盈时间大于2秒），皮肤花纹，粘膜苍白或发绀，尿量小于30ml/
26、h或无尿；收缩压小于90mmHg；脉压小于30mmHg；原有高血压者收缩压较原有水平下降30以上。凡符合、中的二项，和、中的一项者，即可成立诊断。,休克的诊断，一般不难。重要的是要作出早期诊断。待到血压下降才诊断休克，有时可能已经太晚。凡遇到大量失血、失水或严重创伤时，均应想到休克发生的可能。在观察过程中，如果发现患者有精神兴奋、烦躁不安、出冷汗、心率加快、脉压缩小、尿量减少等，则应认为已有休克。如果患者口渴不止，神志淡漠，反应迟钝，皮肤苍白，出冷汗，四肢发凉，呼吸浅而快，脉搏细速，收缩压降至12kPa(90 mmHg)以下和少尿等，则应认为已进入休克抑制期。至于感染性休克的诊断，可根据病人有
27、严重感染的存在，又出现休克代偿期的某些临床表现，或突然出现明显的过度换气来考虑。高阻力型感染性休克具有一些常见的休克表现，诊断不难。但低阻力型感染性休克病人缺少这些常见的休克表现，诊断比较困难，尚需进行一些特殊检查，才能确定诊断。,特别注意,Management of Shock,ABCs still apply must address the underlying causerestore circulation in addition, treat consequences of circulatory disturbance (acidosis, hypothermia, coagul
28、opathy, hypocalcaemia, electrolytes),Management of Shock (II),ventilationcirculationvolumeafterload (reduce if adequate BP)drugs (vasopressors, inotropes)mechanical (e.g. IABP, decompress tamponade),治疗原则,1.一般紧急治疗2.补充血容量3.积极处理原发病4.纠正酸碱平衡失调5.改善低氧血症6.血管活性药物的应用7.治疗DIC改善微循环8.皮质类固醇和其他药物的应用,Principle:Early
29、 Recognition- Do not relay on BP! (30% fluid loss)Control hemorrhageRestore circulating volumeOptimize oxygen delivery DO2600 ml/min.m2 VO2170 ml/min.m2 CI4.5L/min.m2Vasodilator if BP still low after volume loading,Treatment of Shock,Seldom use only vasoconstrictorVasodilator and volume expansion th
30、erapyCombined application of vasodilator and vasoconstrictor,Current Pharmacotherapy of shock:,Hemodynamic monitoring,1. Mental status：brain tissue perfusion2. Skin perfusion：warm, normal color good perfusion cold, pale, moist skin vasoconstriction3. Blood pressure：important but no sensitive indexEa
31、rly detection : Dont rely on BPsystolic pressure12 kPa (90 mmHg) pulse pressure2.67 kPa (20 mmHg),General monitoring（5 item）,4. Pulse rate： Initial presentation of shock： increased pulse ratesShock index： PR/SP mmHg 0.5 no shock，1.0-1.5 shock，2.0 severe shock5. Urine output： the most sensitive index
32、 of the adequacy of vital organ perfusionoliguria：initial shock , initial resuscitationnormal BP, oliguria and low specific gravity： acute renal failure(ARF)urine output 30ml/h：improve,Special monitoring（6 item）,1. Central Venous Pressure (CVP): CVP = right atrial pressure (RAP) = right-ventricular
33、end-diastolic pressure (RVEDP) (Right Ventricular Preload) a valuable guide to vascular volume repalcement Normal CVP 0.490.98kPa(5 10cmH2O) A rising CVP indicates filling of the venous reservoir restoration of total intravascular volume or cardiac failure A falling CVP indicates depletion of the ve
34、nous reservoir 2. Pulmonary Capillary Wedge Pressure (PCWP): PCWP = left atrial pressure (LAP) = left-ventricular end-diastolic pressure (LVEDP) (Left Ventricular Preload) Normal volume 0.82kPa(6 15 cmH2O),CVP AND CIRCULATING VOLUME?,Pulmonary Artery Catheterization,Klkj,3. Cardiac Output (CO) = HR
35、SV (L/min) Normal CO = 4 to 6 L/min It measured with the Swan-Ganz baloon catheter4. Cardiac Index (CI) = CO/BSA (L/min/m2) Normal CI = 2.5-3.5 L/min/m2Oxygen delivery （DO2）: 1.34HBCO10SaO2Oxygen uptake（VO2): 1.34HBCO10(SaO2-SvO2）,5. Arterial blood gas analysis：PaO2 : 10.713Kpa(80100mmHg) PaCO2: 4.8
36、5.8Kpa(3644mmHg) arterial pH: 7.357.45Reflected repiratory reverse, ARDS, acid-base balance, acidosis, et al6. Serum lactate levels：as a prognostic guidenormal value 11.5 mmol/Lheavy patient 2 mmol/Lexceed 8 mmol/L: a mortality rate of 100,低血容量性休克（hypovolemic shock）,一、失血性休克（hemorrhagic shock） 原因: 治疗
37、原则：补充血容量 积极处理原发病 制止出血二、创伤性休克（traumatic shock） 原因: 治疗原则：补充血容量 纠正酸碱平衡失调 手术治疗 药物,失血量的判断,休克指数脉搏/收缩压，0.5，说明正常或失血量为10%；1.0，说明失血量约为20%30%；1.5，说明失血量约为30%50%；收缩压80mmHg，失血量约在1500ml以上；凡有以下一种情况，失血量约在1500ml以上：苍白、口渴；颈外静脉塌陷；快速输平衡液1000ml，血压不回升；一侧股骨开放性骨折或骨盆骨折。,中心静脉压与补液的关系,CVP BP 原因 处理原则 低 低 血容量严重不足 充分补液低 正常 血容量不足 适当补液高 低 心功不全或 强心药，纠酸 血容量相对过多 舒张血管 高 正常 容量血管过度收缩 舒张血管正常 低 心功不全或血容量不足 补液试验*补液试验：取等渗盐水250ml，于510分钟内经静脉注入。如血压升高 而中心静脉压不变，提示血容量不足；如血压不变而中心静 脉压升高0.290.49kpa(35cmH2O)，则提示心功能不全。,sorry ,I am not good at English. Thank you very much!,
